ArticleMolecular cancer research : MCR2017
A Genome-Wide Loss-of-Function Screen Identifies SLC26A2 as a Novel Mediator of TRAIL Resistance.
Article in Molecular cancer research : MCR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- SLC26A2 as a key regulator and therapeutic target in hepatocellular carcinoma: evidence from pan-cancer and mechanistic studies.Human genomics · 2026Article
- Stromal transcriptomics uncover LIF as a key effector in high tumor budding triple-negative breast cancer.Scientific reports · 2025Article
- A deep learning model to predict glioma recurrence using integrated genomic and clinical data.Communications medicine · 2025Article
- Substrate binding plasticity revealed by Cryo-EM structures of SLC26A2.Nature communications · 2024Article
- Discovering the anti-cancer potential of non-oncology drugs by systematic viability profiling.Nature cancer · 2020Article
- Suppressing UPR-dependent overactivation of FGFR3 signaling ameliorates SLC26A2-deficient chondrodysplasias.EBioMedicine · 2019Article
- X-linked inhibitor of apoptosis inhibition sensitizes acute myeloid leukemia cell response to TRAIL and chemotherapy through potentiated induction of proapoptotic machinery.Molecular oncology · 2018Article
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10 authors.
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Abstract
TRAIL is a potent death-inducing ligand that mediates apoptosis through the extrinsic pathway and serves as an important endogenous tumor suppressor mechanism. Because tumor cells are often killed by TRAIL and normal cells are not, drugs that activate the TRAIL pathway have been thought to have potential clinical value. However, to date, most TRAIL-related clinical trials have largely failed due to the tumor cells having intrinsic or acquired resistance to TRAIL-induced apoptosis. Previous studies to identify resistance mechanisms have focused on targeted analysis of the canonical apoptosis pathway and other known regulators of TRAIL receptor signaling. To identify novel mechanisms of TRAIL resistance in an unbiased way, we performed a genome-wide shRNA screen for genes that regulate TRAIL sensitivity in sublines that had been selected for acquired TRAIL resistance. This screen identified previously unknown mediators of TRAIL resistance including angiotensin II receptor 2, Crk-like protein, T-Box Transcription Factor 2, and solute carrier family 26 member 2 (SLC26A2). SLC26A2 downregulates the TRAIL receptors, DR4 and DR5, and this downregulation is associated with resistance to TRAIL. Its expression is high in numerous tumor types compared with normal cells, and in breast cancer,
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